Exposure to UV radiation can cause erythema (sunburn), the formation of DNX pyrimidine dimers, premature ageing and dermal connective tissue changes. It is common to evaluate the protection from erythema provided by a sunscreen preparation by determining its sunscreen protection factor (SPF). The practice, of determining SPF is useful not only in providing information as to the effectiveness of different sunscreen preparations in protecting against erythema, but also in the determination of a minimum level of protection which must be met before a given sunscreen preparation can be marketed commercially.
Studies have shown that exposure to ultraviolet radiation can also profoundly impair the cutaneous immunity of mammals and it is widely believed that ultraviolet radiation induced immunosuppression contributes significantly to cutaneous carcinogenesis.
The effects of UV radiation on the immune system include reduced contact hypersensitivity (CHS) and delayed hypersensitivity reactions, systemic immunosuppression in mice, and tolerance of tumours in mice or epicutaneous antigens in humans Noonan 1981, Hersey 1983, Ullrich 1986, Cestari 1995, Cooper 1992!. In humans, such alterations in immunity can occur even with small, suberythemal doses of UV.
Where cutaneous immunity is markedly affected by long-term, systemic immunosuppressive medications, as is seen in transplant recipients, the incidence of non-melanoma skin cancer is ten to one hundred-fold higher than in age-matched, immunologically competent controls London 1995, Espana 1995!.
It is, therefore, important that human beings who are exposed to even small doses of UV radiation be protected not only from the erythemal and mutagenic effects of sunlight, but also from its immunosuppressive effects. While sunscreens can decrease the formation of pyrimidine DNA dimers Freeman 1988!, reduce the incidence of pre-malignant solar keratoses Thompson 1993, Naylor 1995!, can delay and even prevent UV tumorigenesis in mice Kligman 1980!, and may help reduce the incidence of skin cancer in humans, if they fail to protect the immune system then individuals using high SPF sunscreens who tend to stay in the sun for extended periods may become severely immunosuppressed and have an increased risk of skin malignancy.
Recently, Whitmore et al 1995! found that a high SPF sunscreen completely prevented UV suppression of induction of primary contact sensitisation to dinitrochloroberizene (DNCB). Work in mice suggests that UV immunoprotection is more dependent on broad spectrum cover than SPF Bestak 1995!, since the erythemal and immunosuppressive spectra are probably different.
Previous studies of UV suppression of CHS have used induction of primary CHS to antigens such as DNCB. However, since induction of primary CHS requires exposure to an antigen for the first time the immune response to the antigen cannot be anticipated and it is possible the exposure may elicit a severe response which is, of course, undesirable.
Induction of primary CHS to an antigen also necessarily means that the resultant immune response may only be evaluated once in a given subject. Accordingly, in order to evaluate the ability of a substance to suppress a skin immune response or to evaluate the protection provided by the substance against suppression of the immune response by ultraviolet radiation using induction of primary CHS, a large number of different individuals are required. This is also undesirable and is compounded by the need to use different groups of individuals each time a substance is evaluated.
With the increasing availability of high SPF sunscreens, such as SPF 30, which encourages individuals to stay in the sun for substantial periods of time, there is a need for a reliable and relatively convenient method for evaluating the amount of immunoprotection afforded by commonly used sunscreen ingredients and sunscreens in general. Similarly, there is a need for a suitable and effective method for evaluating whether the cutaneous immunity of an individual is impaired by a substance when applied to the individual's skin.